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J Biol Chem, Vol. 274, Issue 16, 11022-11029, April 16, 1999
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From the Cyclin G, a recent addition to the cyclin family,
was initially identified in screens for new src kinase
family members and soon thereafter by differential screening for
transcriptional targets of the tumor suppressor gene, p53.
We have identified cyclin G as being overexpressed in breast and
prostate cancer cells using differential display polymerase chain
reaction screening. We demonstrate here that cyclin G is overexpressed
in human breast and prostate cancer cells and in cancer cells in
situ from tumor specimens. Cyclin G expression was tightly
regulated throughout the cell cycle in normal breast cells, peaking at
the S and G2/M phases of the cell cycle with lower levels
in G1. The cell cycle-dependent expression was
absent in breast cancer cells. Following DNA damage in normal p53+/+
cells, cyclin G is triggered to cluster in discrete nuclear DNA
replication foci that contain replication-associated proteins such as
proliferating cell nuclear antigen (PCNA). While p53 Department of Medicine, Beth Israel
Deaconess Medical Center, Harvard Institutes of Medicine, Harvard
Medical School, Boston, Massachusetts 02115 and the Derald H. Ruttenberg Cancer Center, Mount Sinai School of Medicine,
New York, New York 10029
/ cells
displayed a faint cyclin G nuclear staining pattern, there was no
increased expression and no change in distribution of the staining
pattern after DNA damage. The specific subcellular localization of
cyclin G at DNA replication foci provides an additional link between
p53-mediated growth arrest and cell cycle regulation and suggests that
cyclin G may act as an effector of p53-mediated events by functional
association with replication foci protein(s).
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